Oxygen consumption after cardiopulmonary bypass - implications o of different measuring methods

Objective: To determine whether intra-pulmonary oxygen consumption or whole body oxygen consumption is the main determinant of the hypermetabolic response after cardiopulmonary bypass. Secondly, which method of measuring oxygen consumption best quantifies this hyperdynamic response. Design: We measured oxygen consumption by analysing respiratory gas (VO2-gas), carbon dioxide excretion (VCO2), and respiratory exchange ratio (RER = VCO2/VO2), and calculated oxygen consumption using the Fick-method (VO2-Fick) and intra-pulmonary oxygen consumption (VO2-gas - VO2-Fick) in patients at fixed times before and after elective cardiac surgery. Next, comparisons were made between methods and also between measurements at different times before and after bypass. Setting: University hospital Patients: 10 elective cardiac surgical patients Interventions: None Measurements and results: VO2-gas, VCO2 and RER were measured with an open circuit indirect calorimeter VO2-Fick was calculated: VO2-Fick=cardiac indexx(arterial - mixed venous oxygen content). Intrapulmonary oxygen consumption was calculated as the difference between VO2-gas and VO2-Fick. Both VO2-gas and VO2-Fick were about 20% higher after bypass than after induction of anaesthesia. Absolute values of VO2-gas were about 30% higher than VO2-Fick. Intra-pulmonary oxygen consumption accounted for 32% of whole body oxygen consumption after induction of anaesthesia and did not increase after bypass. Conclusion: Whole body oxygen consumption and not intra-pulmonary oxygen consumption is the main determinant of the hypermetabolic response after bypass. Increased intra-pulmonary oxygen consumption is not related to bypass. VO2-gas best quantifies this hypermetabolic response directly after bypass, and not VO2-Fick, VCO2 or intra-pulmonary oxygen consumption, since VO2-Fick excludes intra-pulmonary oxygen consumption and VCO2 does not reflect metabolism directly after bypass

THE ROLE OF DIFFERENT TYPES OF CORTICOSTEROIDS ON THE INFLAMMATORY MEDIATORS IN CARDIOPULMONARY BYPASS

In a placebo-controlled double-blind study on patients undergoing cardiopulmonary bypass (CPB) we studied the inhibited effects of dexamethasone, a high dose of methylprednisolone, and a low dose of prednisolone on the inflammatory reaction induced by CPB. During CPB two episodes of blood activation were noticed. First, the blood-material interaction caused a significant increase in complement C3a and elastase concentrations after the start of bypass (p <0.01). Secondly, the reperfusion of the ischemic heart, lungs, and peripheral tissue, after the release of the aortic cross-clamp, caused an additional increase in C3a and elastase concentration and a statistically significant increase in leukotriene B4 (LTB4) concentration and tissue plasminogen activator (t-PA) activity (p <0.01, p <0.05, respectively). Dexamethasone treatment effectively inhibited the increase in LTB4 concentration and t-PA activity after release of the cross-clamp (significant differences to the placebo group, p <0.01, p <0.05, respectively). High-dose methylprednisolone treatment was almost as effective as dexamethasone treatment, whereas low-dose prednisolone treatment was less effective that methylprednisolone in the inhibition of the inflammatory mediators (DM > MP > P). None of the corticosteroid regimens was able to inhibit the increase in complement C3a and elastase. We therefore conclude that corticosteroids do not have an effect on complement activation during CPB. However, leukocyte activation and t-PA activity after release of the aortic cross-clamp are effectively inhibited by corticosteroid treatment, in a dose-dependent way. The inhibition of this inflammatory reaction will have a favourable effect on the postoperative course in patients who have undergone CPB